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Infection and Immunity, May 2007, p. 2399-2407, Vol. 75, No. 5
0019-9567/07/$08.00+0     doi:10.1128/IAI.01563-06
Copyright © 2007, American Society for Microbiology. All Rights Reserved.

Induction of Human ß-Defensin 2 by the Probiotic Escherichia coli Nissle 1917 Is Mediated through Flagellin{triangledown}

Miriam Schlee,1 Jan Wehkamp,1,2 Artur Altenhoefer,3 Tobias A. Oelschlaeger,3 Eduard F. Stange,2 and Klaus Fellermann2*

Dr. Margarete Fischer Bosch Institute of Clinical Pharmacology, Stuttgart, Germany,1 Department of Internal Medicine I, Robert Bosch Hospital, Stuttgart, Germany,2 Institute of Molecular Biology of Infection, University of Würzburg, Würzburg, Germany3

Received 28 September 2006/ Returned for modification 21 November 2006/ Accepted 24 January 2007

Human ß-defensin 2 (hBD-2) is an inducible antimicrobial peptide synthesized by the epithelium to counteract bacterial adherence and invasion. Proinflammatory cytokines, as well as certain bacterial strains, have been identified as potent endogenous inducers. Recently, we have found that hBD-2 induction by probiotic Escherichia coli Nissle 1917 was mediated through NF-{kappa}B- and AP-1-dependent pathways. The aim of the present study was to identify the responsible bacterial factor. E. coli Nissle 1917 culture supernatant was found to be more potent than the pellet, indicating a soluble or shed factor. Chemical analysis demonstrated the factor to be heat resistant and proteinase digestible. Several E. coli Nissle 1917 deletion mutants were constructed and tested for their ability to induce hBD-2 expression in Caco-2 cells. Deletion mutants for flagellin specifically exhibited an impaired immunostimulatory capacity. Reinsertion of the flagellin gene restored the induction capacity to normal levels. Isolated flagellin from E. coli Nissle 1917 and from Salmonella enterica serovar Enteritidis induced hBD-2 mRNA significantly in contrast to the flagellin of the apathogenic E. coli strain ATCC 25922. H1 flagellin antiserum abrogated hBD-2 expression induced by flagellin as well as E. coli Nissle 1917 supernatant, confirming that flagellin is the major stimulatory factor of E. coli Nissle 1917.

* Corresponding author. Mailing address: Robert Bosch Hospital, Department of Internal Medicine I, Auerbachstr. 110, 70376 Stuttgart, Germany. Phone: 49/711-8101-3487. Fax: 49/711-8101-3793. E-mail: klaus.fellermann{at}rbk.de

{triangledown} Published ahead of print on 5 February 2007.

Editor: A. D. O'Brien

Infection and Immunity, May 2007, p. 2399-2407, Vol. 75, No. 5
0019-9567/07/$08.00+0     doi:10.1128/IAI.01563-06
Copyright © 2007, American Society for Microbiology. All Rights Reserved.



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